2. Nephrology SMLE 2023 ✅.pdf

Nephrology SMLE review 2023 Elaf Faisal Obaid PGY-4 Internal Medicine Senior Resident Alnoor specialist hospital - Makkah Last update on 3 August 2023 Topics:1- Acute kidney injury 2- Chronic kidney diseases 3- Glomerular diseases 4- Hypertension in CKD 5- Electrolytes disorders 6- Nephrolithiasis 7...

Nephrology SMLE review 2023 Elaf Faisal Obaid PGY-4 Internal Medicine Senior Resident Alnoor specialist hospital - Makkah Last update on 3 August 2023 Topics:1- Acute kidney injury 2- Chronic kidney diseases 3- Glomerular diseases 4- Hypertension in CKD 5- Electrolytes disorders 6- Nephrolithiasis 7- Urinary tract infections ||.. Acute kidney injury.. || Most common cause AKI in Outpatient is pre renal : hypotension, vomiting, diarrhea, gastroenteritis, Most common hospital acquired AkI is Acute tubular necrosis bec medication or prolonged pre renal Two drugs cause AKI: NSAID: vasoconstriction afferent so dec blood flow to renal ACEI: vasodilation efferent so inc blood flow from renal Normally function of renal reabsorption of Na and excretion K Pathophysiology Renal function test: Creatinine: measured function renal self BUN: increased by pre-renal bec dehydrate FENa: Excretion of Na and reabsorption K What’s the cause of isolated high BUN with normal creatinine ? Upper GI Bleeding ! - Pre-renal (If prolonged will lead to acute tubular necrosis) Increased BUN:creatinine ratio > 20 hypotension= Dec blood flow likes stenosis , obstruction blood flow of kidney, blood volume in body reduces (hemorrhage shock, hypovolemic shock, heart failure), sepsis FENa (%) (fractional excretion of Na) < 1% - Renal Decreased BUN:creatinine ratio Acute tubular necrosis, Rhabdomyolysis FENa (%) (fractional excretion of Na) > 2% - Post-renal (Obstruction at any site from renal tubule to the urethra) Increased BUN : Creatinine ratio >20 Acute tubular necrosis - Due to drug, toxin or prolonged pre-renal state - Most common cause of hospital acquired AKI - Presence of Muddy brown cast or granular cast Or epithelial cell - Urine Na high - FeNa > 2% Urine microscopy (very important):- RBCs Cast or dysmorphic red cells indicates glomerulonephritis Muddy brown or granular cast in ATN Hyaline cast in pre-renal causes WBC cast indicates infection or interstitial nephritis Fatty cast in nephrotic syndrome Waxy cast in chronic kidney disease Acute interstitial nephritis - Triad of eosinophilia, fever and rash - Presence of pyuria and eosinophiluria - Review patient’s medications list - Eosinophiliuria DDx:- AIN and cholesterol emboli Recently did PCI then comew pt with AKI + livedo reticularis rash Rhabdomyolysis Muscle injury bec crush injury or in run marathon " Muscle when injured releases Myoglobin it’s toxic for kidneys - Dark tea color urine with dipstick +ve for blood but no erythrocyte on UA - Following heat exposure or crush injury - High CK level - Treatment:- IV fluid Contrast induced nephropathy - Increased serum creatinine within 24 to 48 hours following contrast exposure - High risk for CIN:- recent AKI, eGFR < 30 - Only approved prophylaxis is IV 0.9 saline and use of isoosmolar or low osmolar contrast - No benefit of N-acetylcystine, dialysis post-contrast or sodium bicarbonate infusion Acute ||.. Indication for renal replacement therapy.. || 1- Refractory hyperkalemia 2- Refractory fluid overload 3- Refractory acidosis 4- Uremic pericarditis or uremic encephalopathy 5- Intoxication When he mention Medication in case should be either Acute interstitial nephritis or Acute tubular necrosis , so how i well differentiate by type of urine Cast red WBC cast Pt marathon run , crash injury or after seizure Hemolytic uremic syndrome i mpearied vena RBC Cast, new onset of hypertension Acute tubular necrosis Pre-renal Glomerulonephritis Acute ||.. Chronic kidney diseases.. || Small kidneys on ultrasound suggest chronicity except in:1- DM 2- HIV 3- Polycystic kidney disease 4- Amyloidosis The kidneys will preserve its size N.B: most common cause of death in ESRD patient is cardiovascular diseases Diabetic nephropathy - Protein > 3.5 Gm in diabetic patient - Clinical diagnosis, absence of diabetic retinopathy make it unlikely cause of proteinuria - Screen with albumin/creatinine ratio annually starting from:At time of diagnosis for Type 2 DM 5 years after diagnosis for Type 1 DM Same fundus exam - Treatment:BP and glucose control ACE inhibitors or ARBs I Pril Sartan IF Diabetic pt have protein in urine when do renal biopsy? IF Pt knows of uncontrolled DM and have before micro or macrovascular complications especially diabetic retinopathy i can diagnose him by diabetic nephropathy without renal biopsy. IF Pt knows of uncontrolled DM and i do fundus examination and I don’t found diabetic retinopathy here may i do renal biopsy Delaying progression of CKD:1- BP control 2- Glycemic control 3- ACEi in case of proteinuria 4- SGLT-2 inhibitors (Empagliflozin) 5- Low protein diet (but not restricted and not in case of nephrotic syndrome) 6- Sodium bicarbonate only in case of metabolic acidosis Anemia in chronic kidney disease:- Anemia of chronic inflammation, treated with SC Erythropoietin - Iron deficiency anemia should be ruled out first and if present to be treated first - Transferrin saturation < 20% + Ferritin < 100 à Iron supplement - Transferrin saturation > 20% + Ferritin > 100 à SC Erythropoietin - EPO in contraindicated in case of malignancy - Target hemoglobin in CKD:- 10 – 11.5 - One of side effects of EPO is hypertension Dialysis Disequilibrium Syndrome Range of systemic and neurological symptoms occurs during dialysis especially in patients in whom dialysis is initially started Nausea, vomiting, headache, restlessness, seizure, coma Due to rapid shift of urea causing rapid lowering in serum osmolarity HbA1C 8.5 is acceptable if : old age or recurrent hypoglycemia attack or end stage. Otherwise should be less 7 Target BP in diabetic is 130/80 Same RA and SLE Anemia in CKD may by anemia of chronic inflammation: bc Erythropoietin deficiency (Erythropoietin hormones release from kidney work in bone marrow maked release more reticulocyte more RBC if kidney affected erythropoietin lose lead to anemia) so tx is erythropoietin subcutaneous but after make sure not caused by iron deficiency anemia So first step do iron study First step with pt has high creatinine is Check previous creatinine to differentiate between CKD and AKI: If pt had abnormal creatinine before 3 months this is CKD. If I don’t have previous readings for creatinine can differentiate by US to know size of kidney, normocytic anemia (anemia of chronic inflammation from CKD), phosphorus and calcium (secondary hyperparathyroidsium bec kidney release ca outside so send impulse (low Ca) to parathyroid no Ca so high parathyroid, by time parathyroid hyperplasia and release high amounts hormones to compensation Ca Here turn to Tertiary hyperparathyroidsium (Ca high) Not Order in CKD or anemia, only when polycythemia, high hg Best way for dialysis: less infections, but need 6 months to mutation. So not used in emergency cases Every year If already stablish diabetics nephropathy (there is protein and albumin in urine) this indicates start ACEI bec dec progression of albuminuria Not in prevention, it’s used for diagnostic nephrotic syndrome (edema + urine protein more than 3.5g) Then reassess ||.. Glomerular diseases.. || Nephrotic vs Nephritic syndrome Nephrotic syndrome Nephritic syndrome Protein in 24 hours urine > 3.5 Gm < 3.5 Gm Urine cast Fatty cast RBCs cast Clinical symptoms Generalized edema, peri-orbital edema Hypertension Hyperlipidemia Yes No Minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, diabetic nephropathy All other Diseases All needs kidney biopsy to confirm diagnosis except diabetic nephropathy it is clinical diagnosis Hints to diagnose Nephrotic syndrome in MCQs Minimal change disease:- most common in children, excellent response to steroid Membranous nephropathy:- associated with SLE, cancer (solid tumor or lymphoma), infections (HCV, HBV, syphilis or malaria), drugs like NSAIDs, strong association with thrombosis especially renal vein thrombosis, positive phospholipase A2 receptor antibody Focal segmental glomerlosclerosis:- Obese, black, HIV, Heroin use Diabetic nephropathy:- long-standing uncontrolled DM with presence of retinopathy To decrease protein in all nephrotic syndrome use ACEi except in minimal change disease treat the underlying cause with Prednisone IgA nephropathy presented within 3 days of URTI Post-infectious glomerulonephritis —> 10 days after a streptococcal throat infection or longer after a skin infection 90% of PSGN cases has low C3 and CH50 within first 2 weeks Returned to normal again within 4-8 weeks C4 is usually within normal Causes of glomerulonephritis associated with low serum complements: Post-infectious glomerulonephritis Subacute bacterial infection, especially endocarditis Systemic lupus erythematosus Cryoglobulinemia Membranoproliferative glomerulonephritis Alport syndrome Sensorineural hearing loss + Ocular findings (lenticonus) In presence of family Hx of ESRD Inherited defect in collagen Type 4 Infective endocarditis ||.. Hypertension in CKD.. || Keywords for HTN in MCQs:1- ACEI + ARBS are contraindicated together 2- ACEI + ARBS during pregnancy are contraindicated 3- ACEI is contraindicated in bilateral renal artery stenosis but can be used if unilateral 4- HTN + DM = ACEI 5- HTN + CKD = ACEI 6- Beta blockers should not be used as a 1st line treatment except in case of CAD 7- Avoid using CCB in patient with heart failure 8- Labetalol is the best for HTN in pre-eclampsia Renal artery stenosis Fibromuscular dysplasia + early onset hypertension (especially in women) + Atherosclerotic stenosis + flash pulmonary edema + asymmetrical kidneys on US + rapid deterioration of RFT after using of ACEI + bruit near the umbilicus Next step: Doppler US Definitive diagnosis: CT angiography Hypokalemia Family hx, Us showed cyst ||.. Electrolytes disorders.. || Drugs causing high K level:β blockers ACE inhibitors ARBs Calcineurin inhibitors (cyclosporine) Spironolactone Eplerenone Amiloride Heparin NSAIDs Na symptoms : mainly Neurological (seizures, coma, convulsion) K Symptoms: mainly Muscular symptoms ( muscle weakness, functional weakness, paralytic ileus) more than neurological symptoms Muscle and Cardiac arrest bec hyperkalemia or hypokalemia ‫اكثر خوفي من بوتاسيوم‬ Potassium concentrations < 6.5 mmol/L in the absence of neuromuscular symptoms or ECG changes —> reduction of potassium intake and correction of predisposing factors In acute and/ or severe hyperkalemia (plasma potassium > 6.5–7.0 mmol/L) For heart stabilization only Dec K level To correct acidosis By kidney or GI tract Causes diarrhea If refractory hyperkalemia Alkalosis Cause hypokalemia Acidosis Cause hyperkalemia Normal K level : 3.5 - 5.3 Hypokalemia in MCQs - Common causes of hypokalemia:- vomiting, diarrhea, alkalosis or diuretics And Beta agonists - Clinical presentation:- muscle weakness, paralytic ileus, flat T wave or U wave on ECG - Treatment:K level > 3 and patient can tolerate orally à Potassium chloride tablet K level < 3 or can not tolerate orally à Potassium chloride IV Or refractory hypocalcemia - In case of refractory hypokalemia despite correction à Check Mg level and correct first if deficient ECG changes in Hyperkalemia vs Hypokalemia Peaking of the T wave is an early ECG sign progressed to widening of the QRS complex Flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression Tumor lysis syndrome Occurs when a large number of cancer cells destructed within a short period releasing its content into the blood Typically associated with bulky rapidly proliferating tumors (e.g. acute leukemia or Burkitt lymphoma), post chemotherapy All are hyper (Hyperkalemia, Hyperuricemia, Hyperphosphatemia) except Calcium it will be low (Hypocalcemia) Treatment:- IV hydration / Rasburicase (check for G6PD level first) Prophylaxis:Hydration + Allopurinol for low risk group Rasburicase for high risk group Renal tubular acidosis:Type 1:- Distal, hypokalemia, nephrolithiasis, Sjogren syndrome, SLE Type 2:– Proximal, hypokalemia, multiple myeloma, Fanconi syndrome Type 4:- Distal, hyperkalemia, renal parenchymal disease All has normal anion gap metabolic acidosis + positive urine anion gap Na normal level 135-145 Hyponatremia: Less than 135 Ifnotmlmole antbsp gig 2Na+BUN+glucose e hypergiacenia wino any corrected income glucose Psudohyponatremia Multiple myeloma ask.name is come with nanogo s so is once wasooo ios eonto 2u was a glucose True-hyponatriuma so oooo saz to Bo lotizo neonate a msn.sc we Pt critical ill, icu, Legionella pneumonia, antipsychotic medication. Dec urine output Inc urine output Tx: saline isotonic 0.9% ACH, TSH, T3 ,T4, Fluid restriction Tx: Diuretic + fluid restriction Management of hyponatremia:- - SIADH à Fluid restriction - Symptomatic à 3% saline - Hypovolemic and no symptoms à 0.9 % NS - Hypervolemic à Lasix + fluid restriction Rate of Na correction in hyponatremia not to exceed 6-8 per day Rapid correction of hyponatremia may cause Osmotic demyelination syndrome (previously known as central pontine myelinolysis) While rapid correction of hypernatremia may cause Cerebral edema Heparin inc PTT Warfare inc INR Anorexia nervosa : have below BMI , have many complications: superior mesenteric artery syndrome, malnutrition , recurring infections. This pt when admitted hospital start initial nutrition , once start feedings after prolonged stop eating body start need carbohydrates when he takes insulin secretion so lead to shifts all k mg P intracellular this called refeeding syndrome. How to prevent when start eating little amounts not huge carbs ACEI And Heparin cause hyperkalemia No bec pt new DVT so if i do interpretion coagulation For heart stabilization: any Ecg change by either hypo or hyperkalemia for protection heart This cause diarrhea, so lead hypokalemia For refractory hyperkalemia SIADH If Cns symptoms If hypovolmic hypotonic hyponatremia Should not correction Na more than 8 during 24h bec if rapid increasing will cause CNS distribution How to differentiate between Psychogenic polydipsia and Diabetes insipidus? indirect water deprivation test: If stop water in Psychogenic polydipsia stop urine , if urine still polydispsia is DI Psychogenic polydipsia: hyponatriuma Diabetes insipidus: ADH deficiency bec central cause: neurosurgery operations or crainophrangioma or pituitary tumor or anything in brain then have inc urine output and hypernatriuma , central AHD not releasing (ADH deficiency) from pituitary but if nephrogenic there is ADH but receptors on kidney not work, so give pt ADH if improve mean this deficiency if not improve that mean nephrogenic DI = 3% Saline ||.. Nephrolithiasis.. || Renal stones:Symptoms:- acute flank pain with radiation to groin with hematuria Diagnosis:- CT abdomen without contrast Management is based on size:< or = 5 mm à Pass spontaneously 6-10 mm à Medical treatment (Tamsulosin or Nifedipine) > 10 mm or failure of medical treatment à Urology referral Presence of AKI, pyelonephritis, bilateral obstruction or obstruction of solitary kidney required urgent Urology consultation Renal stones:Hyperparathyroidism + hypercalciuria, Hx of Roux-en-Y surgery à Calcium oxalate Metabolic syndrome + gout à Uric acid Strong family Hx + young age at onset + hexagonal crystal + due to amino acid transport abnormality à Cystine Chronic UTI with urea splitting organism + staghorn calculi à Struvite or Triple phosphate or (magnesium ammonium phosphate) Cystine Stone ||.. Urinary tract infections.. || Do not treat asymptomatic UTI unless pregnant, post transplant or will have urological procedure Choices of antibiotics for UTI:- Trimethoprim-Sulphamethaxazole - Nitrofurantoin - Fosfomycin - Fluoroquinolone (for pyelonephritis) Systemic symptoms: Flank pain, nausea, vomiting, fever Cystitis: local symptoms: dysuria, frequency, hematouria, For non-pregnant women with Sx of uncomplicated cystitis à empirical antibiotic without culture To search of complication: hydronephrosis, perinephric abscess, or stone make obstruction